Search results for "Helium"

showing 10 items of 1689 documents

Influenza virus damages the alveolar barrier by disrupting epithelial cell tight junctions

2016

A major cause of respiratory failure during influenza A virus (IAV) infection is damage to the epithelial–endothelial barrier of the pulmonary alveolus. Damage to this barrier results in flooding of the alveolar lumen with proteinaceous oedema fluid, erythrocytes and inflammatory cells. To date, the exact roles of pulmonary epithelial and endothelial cells in this process remain unclear.Here, we used an in vitro co-culture model to understand how IAV damages the pulmonary epithelial–endothelial barrier. Human epithelial cells were seeded on the upper half of a transwell membrane while human endothelial cells were seeded on the lower half. These cells were then grown in co-culture and IAV wa…

0301 basic medicinePulmonary and Respiratory Medicine030106 microbiologyBiologymedicine.disease_causeVirusCell LineTight Junctions03 medical and health sciencesInfluenza A Virus H1N1 SubtypemedicineInfluenza A virusHumansTight junctionInfluenza A Virus H5N1 SubtypeEpithelial CellsVirologyIn vitroEpitheliumCoculture TechniquesCell biologyPulmonary Alveoli030104 developmental biologymedicine.anatomical_structureCell cultureCytokinesPulmonary alveolusLumen (unit)European Respiratory Journal
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Functional characterization of a novel 3D model of the epithelial-mesenchymal trophic unit

2017

Background/Aim: Epithelial-mesenchymal communication plays a key role in tissue homeostasis and abnormal signaling contributes to chronic airways disease such as COPD. Most in vitro models are limited in complexity and poorly represent this epithelial-mesenchymal trophic unit. We postulated that cellular outgrowth from bronchial tissue would enable development of a mucosal structure that recapitulates better in vivo tissue architecture. Materials and Methods: Bronchial tissue was embedded in Matrigel and outgrowth cultures monitored using time-lapse microscopy, electrical resistance, light and electron microscopy. Cultures were challenged repetitively with cigarette smoke extract (CSE). Res…

0301 basic medicinePulmonary and Respiratory MedicinePathologymedicine.medical_specialtyClinical BiochemistryBronchiRespiratory MucosaBiologyImmunofluorescenceModels Biologicalfibroblastbronchial03 medical and health sciencesIn vivoSmokemedicineHumansFibroblastMolecular BiologyCells CulturedTissue homeostasisMicroscopyMatrigelECMelectron microscopymedicine.diagnostic_testcigarette smokeMesenchymal stem cellEpithelial CellsMesenchymal Stem CellsEpitheliumCell biologyDrug Combinations030104 developmental biologymedicine.anatomical_structurein vitro modelMotile ciliumProteoglycansCollagenLamininepitheliumExperimental Lung Research
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Meta-analysis of gene-environment-wide association scans accounting for education level identifies additional loci for refractive error

2016

Myopia is the most common human eye disorder and it results from complex genetic and environmental causes. The rapidly increasing prevalence of myopia poses a major public health challenge. Here, the CREAM consortium performs a joint meta-analysis to test single-nucleotide polymorphism (SNP) main effects and SNP × education interaction effects on refractive error in 40,036 adults from 25 studies of European ancestry and 10,315 adults from 9 studies of Asian ancestry. In European ancestry individuals, we identify six novel loci (FAM150B-ACP1, LINC00340, FBN1, DIS3L-MAP2K1, ARID2-SNAT1 and SLC14A2) associated with refractive error. In Asian populations, three genome-wide significant loci AREG…

0301 basic medicineRefractive errorgenetic structuresGeneral Physics and AstronomyGenome-wide association studyVARIANTSrefractive error ; geneEYEBioinformaticsINCIDENT MYOPIAGenome-wide association studiesSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]0302 clinical medicinePolymorphism (computer science)10. No inequalityPOPULATIONeducation.field_of_studyMultidisciplinaryQACTIVATED PROTEIN-KINASEta3142single-nucleotide polymorphismRETINAL-PIGMENT EPITHELIUMOUTDOOR ACTIVITY3142 Public health care science environmental and occupational health3. Good healthRefractive errorsMeta-analysislociEducational StatusSciencePopulation610 Medicine & healthEnvironmentBiologyta3111Polymorphism Single NucleotideArticleWhite PeopleGeneral Biochemistry Genetics and Molecular BiologyEducation03 medical and health sciencesAsian PeopleSDG 3 - Good Health and Well-beingGenetic variationmedicineHumansSNPGenetic Predisposition to Diseasemyopia3125 Otorhinolaryngology ophthalmologyGenetic variationeducationRECEPTORGene Expression Profilingta1184General ChemistryHeritabilitymedicine.diseaseeye diseasesta3125TIME OUTDOORS030104 developmental biologyGenetic LociEvolutionary biologyRISK-FACTORS030221 ophthalmology & optometryREsense organs3111 BiomedicineGenome-Wide Association StudyNature Communications
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Subacute effects of ozone exposure on cultivated human respiratory mucosa.

2001

This study was designed to investigate subacute effects of long-term exposure of both healthy and chronically inflamed human respiratory mucosa to ozone. Functional and metabolic effects on ciliary beat frequency (CBF), release of interleukin 8 (IL-8), interleukin 4 (IL-4), and γ interferon (g-INF), as well as cellular viability and cytotoxicity, were monitored. Cell cultures of 60 specimens (healthy mucosa: n = 30, inflamed mucosa: n = 30) were exposed to synthetic air and to ozone-enriched synthetic air in different concentrations of WO, 500, and WOO μg/m3. Continuous expositions were performed using an air/liquid interface cell culture technique for a period of 4 weeks. CBF was monitore…

0301 basic medicineRespiratory MucosaAdultmedicine.medical_specialtyTime FactorsAdolescentMucociliary clearanceCell Survivalmedicine.medical_treatmentRespiratory Mucosa03 medical and health scienceschemistry.chemical_compoundInterferon-gamma0302 clinical medicineOzoneLactate dehydrogenaseInternal medicinemedicineHumansInterleukin 8CiliaCytotoxicityInterleukin 4Cells CulturedAged030102 biochemistry & molecular biologybusiness.industryAirInterleukin-8Middle AgedCytokineEndocrinologyOtorhinolaryngologychemistry030220 oncology & carcinogenesisAnesthesiaRespiratory epitheliumInterleukin-4businessAmerican journal of rhinology
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N-retinylidene-N-retinylethanolamine adduct induces expression of chronic inflammation cytokines in retinal pigment epithelium cells

2021

Blindness due to photoreceptor degeneration is observed in both genetic and acquired eye disorders. Long blue light exposure can contribute to increase levels of oxidative compounds within the retinal pigment epithelium (RPE), enhancing risk of retinal damage. In retina, reactive oxygen species contribute to the activation of inflammatory cascade. If chronic, this inflammatory response can result in photoreceptor death. Therefore, we investigated the effects of the endogenous adduct N-retinylidene-N-retinylethanolamine (A2E) on RPE cells, in order to identify the most dysregulated cytokines and their related inflammatory pathways. RPE cells were exposed to A2E and blue light for 3h and 6h. …

0301 basic medicineRetinal degenerationCell SurvivalInflammationRetinal Pigment Epitheliummedicine.disease_causeA2ECell LineTranscriptomeRetinoids03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineExpression analysiSettore BIO/13 - Biologia ApplicatamedicineHumansInflammationchemistry.chemical_classificationRetinaReactive oxygen speciesRetinal pigment epitheliumSettore MED/30 - Malattie Apparato VisivoChemistryRetinal Degenerationmedicine.diseaseeye diseasesSensory SystemsCell biologyOphthalmology030104 developmental biologymedicine.anatomical_structureGene Expression RegulationChronic Disease030221 ophthalmology & optometryOxidative streCytokinesEye disorderRPEA2E; Expression analysis; Inflammation; Oxidative stress; RPE; Retinal degenerationsense organsmedicine.symptomReactive Oxygen SpeciesRetinal PigmentsOxidative stressSignal TransductionExperimental Eye Research
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Primary Cilium-Mediated Retinal Pigment Epithelium Maturation Is Disrupted in Ciliopathy Patient Cells

2018

SUMMARY Primary cilia are sensory organelles that protrude from the cell membrane. Defects in the primary cilium cause ciliopathy disorders, with retinal degeneration as a prominent phenotype. Here, we demonstrate that the retinal pigment epithelium (RPE), essential for photoreceptor development and function, requires a functional primary cilium for complete maturation and that RPE maturation defects in ciliopathies precede photoreceptor degeneration. Pharmacologically enhanced ciliogenesis in wild-type induced pluripotent stem cells (iPSC)-RPE leads to fully mature and functional cells. In contrast, ciliopathy patient-derived iPSC-RPE and iPSC-RPE with a knockdown of ciliary-trafficking pr…

0301 basic medicineRetinal degenerationInduced Pluripotent Stem CellsRespiratory MucosaRetinal Pigment EpitheliumBiologyCell MaturationCiliopathiesArticleGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciencesCiliogenesismedicineAnimalsCiliaInduced pluripotent stem celllcsh:QH301-705.5Mice KnockoutRetinal pigment epitheliumCiliumRetinal Degenerationmedicine.diseaseCiliopathieseye diseasesCell biologyProtein Kinase C-deltaCiliopathy030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)sense organsCell Reports
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Generation of an inducible RPE-specific Cre transgenic-mouse line.

2018

The retinal pigment epithelium (RPE) is an epithelial monolayer in the back of the vertebrate eye. RPE dysfunction is associated with retinal degeneration and blindness. In order to fully understand how dysregulation affects visual function, RPE-specific gene knockouts are indispensable. Since the currently available RPE-specific Cre recombinases show lack of specificity or poor recombination, we sought to generate an alternative. We generated a tamoxifen-inducible RPE-specific Cre transgenic mouse line under transcriptional control of an RPE-specific Tyrosinase enhancer. We characterized the Cre-mediated recombinant expression by crossing our RPE-Tyrosinase-CreErT2 mouse line with the tdTo…

0301 basic medicineRetinal degenerationMaleEmbryologylcsh:MedicineGene ExpressionRetinal Pigment EpitheliumBiochemistry0302 clinical medicineRecombinaseMedicine and Health Scienceslcsh:ScienceStainingMultidisciplinaryMonophenol MonooxygenaseAnimal ModelsSpecimen preparation and treatmentCell biologyEnzymesmedicine.anatomical_structureExperimental Organism SystemsModels AnimalFemaleAnatomyResearch ArticleGenetically modified mouseImaging TechniquesTransgeneOcular AnatomyMice TransgenicMouse ModelsBiologyResearch and Analysis MethodsRetinaRecombinases03 medical and health sciencesModel OrganismsOcular SystemFluorescence ImagingmedicineGeneticsAnimalsEnhancerGene knockoutRetinaRetinal pigment epitheliumIntegraseslcsh:REmbryosDAPI stainingBiology and Life SciencesProteinsmedicine.diseaseeye diseasesMice Inbred C57BLLuminescent Proteins030104 developmental biologyNuclear stainingEnzymologyAnimal StudiesEyeslcsh:Qsense organsHead030217 neurology & neurosurgeryDevelopmental BiologyPloS one
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Ethanol-Induced Oxidative Stress Modifies Inflammation and Angiogenesis Biomarkers in Retinal Pigment Epithelial Cells (ARPE-19): Role of CYP2E1 and …

2020

The retinal pigment epithelium (RPE) plays a key role in retinal health, being essential for the protection against reactive oxygen species (ROS). Nevertheless, excessive oxidative stress can induce RPE dysfunction, promoting visual loss. Our aim is to clarify the possible implication of CYP2E1 in ethanol (EtOH)-induced oxidative stress in RPE alterations. Despite the increase in the levels of ROS, measured by fluorescence probes, the RPE cells exposed to the lowest EtOH concentrations were able to maintain cell survival, measured by the Cell Proliferation Kit II (XTT). However, EtOH-induced oxidative stress modified inflammation and angiogenesis biomarkers, analyzed by proteome array, ELIS…

0301 basic medicineRetinal degenerationProgrammed cell deathPhysiologyAngiogenesisClinical BiochemistryTerapéuticaretinal pigment epitheliumdegenerationInflammationmedicine.disease_causeFisiologíaDegeneración macularBiochemistryArticle03 medical and health sciencesTratamiento médico0302 clinical medicineMedicina preventivahomeostasismedicineoxidative stressHomeostasisCYP2E1Molecular BiologyRetinal pigment epitheliumchemistry.chemical_classificationReactive oxygen speciesRetinal pigment epitheliumChemistryCell growthlcsh:RM1-950Cell Biologymedicine.diseaseCell biology030104 developmental biologymedicine.anatomical_structurelcsh:Therapeutics. PharmacologyOxidative stress030220 oncology & carcinogenesisDegenerationOftalmologíamedicine.symptomOxidative stress
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The membrane-associated MUC1 improves adhesion of salivary MUC5B on buccal cells. Application to development of an in vitro cellular model of oral ep…

2015

Objectives: The mucosal pellicle is a thin layer of salivary proteins, mostly MUC5B mucins, anchored to epithelial oral cells. This pellicle is involved in protection of oral mucosae against abrasion, pathogenic microorganisms or chemical xenobiotics. The present study aimed at studying the involvement of MUC1 in mucosal pellicle formation and more specifically in salivary MUC5B binding using a cell-based model of oral epithelium. DESIGN: MUC1 mRNAs were not detected in TR146 cells, and therefore a stable cell line named TR146/MUC1 expressing this protein was developed by transfection. TR146 and TR146/MUC1 were incubated with human saliva in order to evaluate retention of MUC5B by epithelia…

0301 basic medicineSaliva[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionEpithelium0302 clinical medicineimmunocytochemistryTR146 cellsDental PellicleOral mucosa[ SDV.MHEP.CHI ] Life Sciences [q-bio]/Human health and pathology/SurgeryMUC1Microscopy ConfocalReverse Transcriptase Polymerase Chain ReactionGeneral MedicineTransfectionImmunohistochemistryMucin-5Bmedicine.anatomical_structuremucosal pelliclescanning electron microscopyImmunoblotting[SDV.MHEP.CHI]Life Sciences [q-bio]/Human health and pathology/SurgeryBiologyIn Vitro TechniquesTransfectionMicrobiologyCell Line03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicineCell AdhesionHumansSalivary Proteins and PeptidesSalivaGeneral Dentistryoral mucosaMucinMucin-1Mouth Mucosa030206 dentistryCell BiologymucinsMolecular biologyIn vitroEpithelium030104 developmental biologyOtorhinolaryngologyCell cultureMicroscopy Electron Scanning[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Programming of Intestinal Epithelial Differentiation by IL-33 Derived from Pericryptal Fibroblasts in Response to Systemic Infection.

2016

SummaryThe intestinal epithelium constitutes an efficient barrier against the microbial flora. Here, we demonstrate an unexpected function of IL-33 as a regulator of epithelial barrier functions. Mice lacking IL-33 showed decreased Paneth cell numbers and lethal systemic infection in response to Salmonella typhimurium. IL-33 was produced upon microbial challenge by a distinct population of pericryptal fibroblasts neighboring the intestinal stem cell niche. IL-33 programmed the differentiation of epithelial progenitors toward secretory IEC including Paneth and goblet cells. Finally, IL-33 suppressed Notch signaling in epithelial cells and induced expression of transcription factors governing…

0301 basic medicineSalmonella typhimuriumCellular differentiationPopulationNotch signaling pathwayMice TransgenicBiologydigestive systemGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineIntestine SmallmedicineAnimalsHumansCell LineageProgenitor cellIntestinal Mucosaeducationlcsh:QH301-705.5Cell Proliferationeducation.field_of_studySalmonella Infections AnimalReceptors NotchCell growthCell DifferentiationEpithelial CellsFibroblastsInterleukin-33Intestinal epitheliumInterleukin-1 Receptor-Like 1 ProteinCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)Organ SpecificityImmunologyPaneth cellSignal transduction030215 immunologySignal TransductionCell reports
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